Abstract
Physical loading raises the sympathetic nervous activity which results in increased minute volume, constriction of peripheral vessels, and elevated blood pressure. These reactions are an outcome of two mechanisms: 1) the central command from cerebral structures that trigger voluntary movements to activate the vasomotor center and 2) the reflexes initiated by mechanic and metabolic changes in a working muscle. The second mechanism of the sympathetic system activation was termed ergoreflex. Ergoreflex controls hemodynamics primarily through activation of mechanosensitive afferents to first of all inhibit the tonic vagal effects on the heart manifested by a leap of heart rate during loading. Activation of chemosensitive afferents comes with some delay in pace with metabolites accumulation in muscles and leads to growth of the efferent sympathetic activity and rise of blood pressure. The metabolic reflex effect is particularly high in the event of muscle fatigue. This review deals with the mechanisms underlying the ergoreflex and their adaptation to hypodynamia, physical loading, and also some pathologies.
Published Version
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